Evidence map›Paper›PMID 22496647›Full record

ArticlePLoS pathogens2012

Regulation of Mycobacterium tuberculosis-dependent HIV-1 transcription reveals a new role for NFAT5 in the toll-like receptor pathway.

Shahin Ranjbar, Luke D Jasenosky, Nancy Chow, Anne E Goldfeld

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
13.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  7. Frontiers in immunology · 2023
    Article
  8. Review
  9. Article
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  11. Article
  12. Review
  13. Article
  14. TheFuture virology · 2020
    Review
  15. Review
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Shahin RanjbarImmune Disease Institute and Program in Cellular and Molecular Medicine, Children's Hospital Boston, Boston, Massachusetts, United States of America.
Luke D Jasenosky
Nancy Chow
Anne E Goldfeld
Boston Children's Hospital · USHarvard University · US

Funding

The impact of HIV viral diversity and cellular immunity on HIV pathogenesisP30AI060354 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ROBERT A. PARKER · 2004 to 2026
$94.4M
Checkpoints of TNF Gene RegulationR01GM076685 · NIGMS · IMMUNE DISEASE INSTITUTE, INC. · PI GOLDFELD, ANNE · 2006 to 2019
$5.2M
HIV-1 regulation by MTb: pathogen and host factorR01AI065285 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI GOLDFELD, ANNE · 2005 to 2009
$2.1M
HIV-1 regulation by MTb: pathogen and host factorR56AI065285 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI GOLDFELD, ANNE · 2010 to 2010
$525k
NIAID NIH HHS AI065285NIAID NIH HHS P30 AI 060354NIAID NIH HHS P30 AI060354NIAID NIH HHS R01 AI065285NIAID NIH HHS R56 AI065285NIGMS NIH HHS GM076685NIGMS NIH HHS R01 GM076685
6 · The paper itself

Abstract

Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression.

Indexed as

Cells, CulturedFemaleGene Expression RegulationHIV-1HIV InfectionsHumansImmunity, InnateInterleukin-1 Receptor-Associated KinasesMaleMycobacterium tuberculosisMyeloid Differentiation Factor 88Promoter Regions, GeneticSignal TransductionToll-Like ReceptorsTranscription FactorsTuberculosisInterleukin-1 Receptor-Associated KinasesIRAK1 protein, humanMYD88 protein, humanMyeloid Differentiation Factor 88NFAT5 protein, humanToll-Like ReceptorsTRAF7 protein, humanTranscription FactorsTumor Necrosis Factor Receptor-Associated Peptides and Proteins

Identifiers

PMID22496647
PMCPMC3320587
OpenAlexW2080111163

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.